Complex Care Study Guide Exam Questions
with Key Marking Scheme Updated
2024/2025
Distributive shock - septic treatment - correct answer Antibiotics, mass amounts of fluids
Obstructive shock (causes/symptoms) - correct answer Partial obstruction to blood flow with
decreased cardiac output --> find obstruction and treat it
Causes:
-Cardiac tamponade (fluid builds up in sac around the heart, can compress the heart) --> use
needle decompression
-Pneumothorax (air in pleural space, causes tracheal deviation) --> fix with chest tube, present if
absence of breath sounds in whichever side
-Superior vena cava syndrome (massive clot or tumor pressing against it)
-Abdominal compartment syndrome (presses on inferior vena cava and causes decreased
blood flow to heart)
-Pulmonary embolus (blood can't get pumped through, causes right-sided heart failure) --> use
blood thinners
Symptoms:
-Decreased cardiac output
-JVD (pulmonary embolus or pneumothorax --> blood backs up)
Initial stage of shock - correct answer Usually not clinically apparent (no symptoms)
Metabolism changes from aerobic (non-oxygen consumption) to anaerobic (massive oxygen
consumption):
-Lactic acid accumulates and must be removed by blood and broken down by liver (this build up
is from lack of tissue perfusion)
-Process requires unavailable O2, unavailable d/t decreased tissue perfusion
,**If we think patient is going sepsis, we will first get lactic acid levels (normal = 0.5-2.0 mmol/L)
Compensatory stage of shock - correct answer Clinically apparent --> body tries to
compensate for consequences of anaerobic metabolism/decreased tissue perfusion and tries to
maintain homeostasis
**Vital signs are changing because sympathetic nervous system is responding --> tachycardia,
vasoconstriction (shunting blood back to heart), cool/pale/clammy extremities, fever, decreased
urinary output, tachypnea (as acid builds, body needs to blow off the CO2, compensates with
tachypnea)
-Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP = stimulates
vasoconstriction, which shunts blood to brain and heart
-↓ blood to kidneys activates renin-angiotensin system (RAS) = renin stimulates angiotensin to
produce angiotensis 1, which uses ACE to convert to angiotensin 2 (potent vasoconstrictor that
causes increase in preload and BP, also stimulates adrenal cortex to release aldosterone, which
reabsorbs sodium/water and excretes potassium) --> increased osmolality --> releases
antidiuretic hormone (ADH) --> further increases blood volume
-Impaired GI motility-risk for paralytic ileus
-Cool, clammy skin from decreased blood flow (assess patient not just monitors)
-Shunting blood from lungs increases physiologic dead space (amount of air that won't reach
gas exchange in units) --> causes a ventilation-perfusion mismatch, arterial O2 levels will
decrease, will have an increase in rate/depth to compensate --> shallow tachypnea
-SNS stimulation increases myocardial O2 demands because it increases cardiac contractility
and heart rate
Progressive stage of shock (look at diagnostic studies we do for shock --> table 66.2, pg 1590) -
correct answer Begins when compensatory mechanisms fail --> need aggressive interventions
to prevent multiple organ dysfunction syndrome
,**Getting worse, body can only compensate for so long --> decrease in UO, mental status
changes, respiratory depression --> might need to intubate patient, ventilator support
-Hallmarks of ↓ cellular perfusion and altered capillary permeability
-Anasarca = diffuse profound edema (fluid moves to extravascular space)
-Movement of fluid from pulmonary vasculature to interstitium (causes increased respiratory rate
initially)
-Fluid moves into alveoli
-Tachypnea, crackles, increased WOB --> eventualy leads to respiratory depression
-CO begins to fall
-Myocardial dysfunction results (MI)
-Mucosal barrier of GI system becomes ischemic --> ulcer, GI bleeding, increases risk of
bacteria migrating from GI tract to blood, decreased inability to absorb nutrients
-Hypoperfusion leads to renal tubular ischemia = acute kidney failure (increase in creatine and
BUN, metabolic acidosis occurs)
-Liver fails to metabolize drugs and waste (lactate & ammonia increases, jaundice results from
increased bilirubin, bacteria that MAY move from GI tract are no longer destroyed by kupferr
cells/macrophages in liver because it's no longer working)
Refractory stage of shock - correct answer -Exacerbation of anaerobic metabolism (from
decreased perfusion from peripheral vasoconstriction & decreased CO)
-Accumulation of lactic acid
, -↑ capillary permeability
-Profound hypotension and hypoxemia
-Tachycardia worsens
-Organ failure --> failure of one organ system affects others
-Recovery unlikely in this stage
Diagnostic studies for shock - correct answer -Thorough history & physical exam
-No single study to determine shock
-Blood studies --> elevation of lactate, base deficit (acid-base balance deficit --> usually
acidotic)
-12-lead ECG of continuous EKG monitoring (look for cardiogenic shock/dysrhythmias)
-Chest x-ray (pulmonary edema, pulmonary embolism, cardiac tamponade)
-Hemodynamic monitoring
Interprofessional care for shock - correct answer Successful management:
-Interventions to control or eliminate the cause of decreased perfusion
-Protection of target and distal organs from dysfunction
-Provision of multisystem supportive care
General management strategies:
with Key Marking Scheme Updated
2024/2025
Distributive shock - septic treatment - correct answer Antibiotics, mass amounts of fluids
Obstructive shock (causes/symptoms) - correct answer Partial obstruction to blood flow with
decreased cardiac output --> find obstruction and treat it
Causes:
-Cardiac tamponade (fluid builds up in sac around the heart, can compress the heart) --> use
needle decompression
-Pneumothorax (air in pleural space, causes tracheal deviation) --> fix with chest tube, present if
absence of breath sounds in whichever side
-Superior vena cava syndrome (massive clot or tumor pressing against it)
-Abdominal compartment syndrome (presses on inferior vena cava and causes decreased
blood flow to heart)
-Pulmonary embolus (blood can't get pumped through, causes right-sided heart failure) --> use
blood thinners
Symptoms:
-Decreased cardiac output
-JVD (pulmonary embolus or pneumothorax --> blood backs up)
Initial stage of shock - correct answer Usually not clinically apparent (no symptoms)
Metabolism changes from aerobic (non-oxygen consumption) to anaerobic (massive oxygen
consumption):
-Lactic acid accumulates and must be removed by blood and broken down by liver (this build up
is from lack of tissue perfusion)
-Process requires unavailable O2, unavailable d/t decreased tissue perfusion
,**If we think patient is going sepsis, we will first get lactic acid levels (normal = 0.5-2.0 mmol/L)
Compensatory stage of shock - correct answer Clinically apparent --> body tries to
compensate for consequences of anaerobic metabolism/decreased tissue perfusion and tries to
maintain homeostasis
**Vital signs are changing because sympathetic nervous system is responding --> tachycardia,
vasoconstriction (shunting blood back to heart), cool/pale/clammy extremities, fever, decreased
urinary output, tachypnea (as acid builds, body needs to blow off the CO2, compensates with
tachypnea)
-Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP = stimulates
vasoconstriction, which shunts blood to brain and heart
-↓ blood to kidneys activates renin-angiotensin system (RAS) = renin stimulates angiotensin to
produce angiotensis 1, which uses ACE to convert to angiotensin 2 (potent vasoconstrictor that
causes increase in preload and BP, also stimulates adrenal cortex to release aldosterone, which
reabsorbs sodium/water and excretes potassium) --> increased osmolality --> releases
antidiuretic hormone (ADH) --> further increases blood volume
-Impaired GI motility-risk for paralytic ileus
-Cool, clammy skin from decreased blood flow (assess patient not just monitors)
-Shunting blood from lungs increases physiologic dead space (amount of air that won't reach
gas exchange in units) --> causes a ventilation-perfusion mismatch, arterial O2 levels will
decrease, will have an increase in rate/depth to compensate --> shallow tachypnea
-SNS stimulation increases myocardial O2 demands because it increases cardiac contractility
and heart rate
Progressive stage of shock (look at diagnostic studies we do for shock --> table 66.2, pg 1590) -
correct answer Begins when compensatory mechanisms fail --> need aggressive interventions
to prevent multiple organ dysfunction syndrome
,**Getting worse, body can only compensate for so long --> decrease in UO, mental status
changes, respiratory depression --> might need to intubate patient, ventilator support
-Hallmarks of ↓ cellular perfusion and altered capillary permeability
-Anasarca = diffuse profound edema (fluid moves to extravascular space)
-Movement of fluid from pulmonary vasculature to interstitium (causes increased respiratory rate
initially)
-Fluid moves into alveoli
-Tachypnea, crackles, increased WOB --> eventualy leads to respiratory depression
-CO begins to fall
-Myocardial dysfunction results (MI)
-Mucosal barrier of GI system becomes ischemic --> ulcer, GI bleeding, increases risk of
bacteria migrating from GI tract to blood, decreased inability to absorb nutrients
-Hypoperfusion leads to renal tubular ischemia = acute kidney failure (increase in creatine and
BUN, metabolic acidosis occurs)
-Liver fails to metabolize drugs and waste (lactate & ammonia increases, jaundice results from
increased bilirubin, bacteria that MAY move from GI tract are no longer destroyed by kupferr
cells/macrophages in liver because it's no longer working)
Refractory stage of shock - correct answer -Exacerbation of anaerobic metabolism (from
decreased perfusion from peripheral vasoconstriction & decreased CO)
-Accumulation of lactic acid
, -↑ capillary permeability
-Profound hypotension and hypoxemia
-Tachycardia worsens
-Organ failure --> failure of one organ system affects others
-Recovery unlikely in this stage
Diagnostic studies for shock - correct answer -Thorough history & physical exam
-No single study to determine shock
-Blood studies --> elevation of lactate, base deficit (acid-base balance deficit --> usually
acidotic)
-12-lead ECG of continuous EKG monitoring (look for cardiogenic shock/dysrhythmias)
-Chest x-ray (pulmonary edema, pulmonary embolism, cardiac tamponade)
-Hemodynamic monitoring
Interprofessional care for shock - correct answer Successful management:
-Interventions to control or eliminate the cause of decreased perfusion
-Protection of target and distal organs from dysfunction
-Provision of multisystem supportive care
General management strategies:
